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Charcot Foot

Original Editor - Chelsea McLene

Top Contributors - Chelsea Mclene, Uchechukwu Chukwuemeka, Kim Jackson, Vidya Acharya, Alexandra Stead and Nikhil Benhur Abburi

Introduction

Charcot neuro-osteoarthropathy (CNO), commonly referred to as Charcot foot, is a severe, progressive inflammatory condition affecting the bones, joints, and soft tissues of the foot and ankle in individuals with peripheral neuropathy.[1] CNO was first described by the French neurologist Jean-Martin Charcot in 1868 in patients with tabes dorsalis, and subsequently recognised in the context of diabetes mellitus in 1936.[2] Today, diabetes mellitus is by far the most common underlying cause, although CNO can also occur in other conditions causing peripheral neuropathy, including chronic renal failure, alcohol-related neuropathy, and leprosy.[1] It is oftentimes a progressive loss of sensation, bone destruction, joint subluxation, and collapse of the medial longitudinal arch that results in the classic "rocker-bottom" deformity. This deformity markedly increases the risk of plantar pressure ulceration, infection, and ultimately major amputation if not treated promptly and appropriately.[3]

[For more information, click here to see the slide video]

Pathophysiology

The pathophysiology of CNO is a complex, multifactorial process, traditionally explained by the convergence of the neurotraumatic and neurovascular theories.[1] The neurotraumatic mechanism involves repetitive, unrecognised micro-trauma to an insensate foot[4], while the neurovascular mechanism suggests that autonomic neuropathy increases blood flow and osteoclast activation.[2]

At the molecular level, this process is driven by the Receptor Activator of Nuclear Factor kappa-Β Ligand (RANKL), Receptor Activator of Nuclear Factor kappa-Β (RANK), and Osteoprotegerin (OPG) pathway. Pro-inflammatory cytokines trigger the activation of NF-κB, which promotes excessive osteoclastogenesis and bone lysis.[4][5] When this accelerated bone destruction is combined with the physical stress of ambulation, it culminates in ligament disruption, joint dislocation, and fractures.[5] Furthermore, genetic predispositions, such as specific polymorphisms within the OPG/RANKL/RANK axis, may increase an individual's susceptibility to these skeletal changes.[3]

Epidemiology

The true prevalence and incidence of Charcot neuro-osteoarthropathy (CNO) remain difficult to characterise due to inconsistent diagnostic reporting. However, contemporary data suggest the condition is far more prevalent than previously assumed. Regional estimates vary from a point prevalence of 0.04% in the UK [2] to a general diabetes prevalence of 0.56% in Denmark,[6] with the lifetime cumulative incidence climbing as high as 13% for those attending diabetic foot clinics.[2] In the United States, annual incidence and prevalence figures have even been shown to surpass those of several common cancers.[6][7]

Also, demographic and clinical profiles from a multicentre study of 761 people with CNO across six countries found that the mean age at diagnosis was 54.5 ± 11.7 years, 71.8% were male, and 83.2% had type 2 diabetes mellitus. Peripheral neuropathy was present in 91.7% of cases, retinopathy in 60.2%, and nephropathy in 45.2%.[8]

Signs and Symptoms

Acute Phase (Active CNO)

Active CNO typically presents as a unilateral, warm, red, and swollen foot in a neuropathic patient.[3] Critically, the clinical appearance is often misleadingly disproportionate to the patient's pain, with many experiencing only mild discomfort or none at all.[2] Symptoms include:

  • Unilateral foot or ankle swelling
  • Erythema (redness) and warmth; skin temperature typically more than 2°C higher than the contralateral foot[9]
  • Absent or disproportionately mild pain (due to peripheral neuropathy)
  • Loss of protective sensation on monofilament testing
  • Reduced or absent vibration perception

Chronic Phase

  • Foot deformity; classically a "rocker-bottom" deformity due to midfoot collapse
  • Bony prominences, particularly at the plantar surface
  • Shortening of the foot
  • Altered gait pattern and reduced mobility
  • Callus formation over bony prominences, predisposing to plantar ulceration
  • Open wound in complicated CNO

CNO, if left untreated, results in deformity, ulceration, infection, and a significant risk of amputation, particularly in cases of uncontrolled infection and chronic ulcers.[10] This emphasises the importance of early diagnosis and care.

Risk Factors

These risk factors are established triggers of CNO, and they include:[2][11][12][13]

  • Peripheral neuropathy (present in over 90% of cases)
  • Long-standing diabetes mellitus (median duration at diagnosis: 15 years)
  • Poor glycaemic control
  • Microvascular complications (nephropathy, retinopathy)
  • History of foot ulceration or foot surgery
  • Male sex (approximately 70% of affected individuals)
  • Obesity and elevated body mass index
  • Autoimmune diseases and non-cancerous thyroid diseases [14]
  • Recent foot or ankle trauma (often unrecognised by the patient)
  • Type 1 diabetes (associated with earlier onset and more severe microvascular involvement)
  • Alcohol or drug abuse
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Stages

Clinical practice utilises two complementary classification systems to guide prognosis and treatment: the Eichenholtz staging system, which defines disease activity, and the Sanders–Frykberg anatomical classification, which identifies the site of involvement. The Eichenholtz classification originally omitted Stage 0, which is a critical omission as this phase is only detectable via MRI. Shibata et al. in 1990 modified this classification to capture this stage. Identifying CNO at Stage 0 is clinically important because it represents the most reversible stage where immediate offloading can successfully prevent the progression of permanent deformity.[12]

Eichenholtz Staging System (Modified by Shibata et al)[12]

Stage Name Clinical Features Radiographic Features
Stage 0 (Shibata modification) Pre-destructive / Prodromal Hot, erythematous, swollen foot; no deformity; often misdiagnosed Normal plain radiograph; bone oedema and stress fractures visible on MRI only
Stage 1 Destruction / Fragmentation Oedema, erythema, warmth; periarticular fragmentation begins Bony debris, periarticular fragmentation, joint subluxation, fracture-dislocation
Stage 2 Coalescence / Healing Reduced oedema and warmth; beginning consolidation Absorption of debris, sclerosis, periosteal new bone formation, sintering of fragments
Stage 3 Consolidation / Remodelling Cool, non-inflamed foot; deformity present but stable Completed bone remodelling; rounded edges; bony fusion

Sanders–Frykberg Anatomical Classification[18]

Type Anatomical Location Frequency
Type I Forefoot (metatarsophalangeal, interphalangeal joints) ~15%
Type II Tarsometatarsal (Lisfranc) joints ~40%
Type III Naviculocuneiform, talonavicular, calcaneocuboid joints ~30%
Type IV Ankle and/or subtalar joint ~10%
Type V Calcaneus (isolated) ~5%

Diagnosis

Diagnosing CNO necessitates a strong clinical index of suspicion when a diabetic patient presents with a unilateral hot and swollen foot. According to IWGDF 2023 guidelines, clinicians should initiate knee-high immobilisation and offloading immediately upon suspicion to prevent further bone destruction, rather than waiting for confirmatory imaging.[3]

Clinical assessment requires a full neurological examination using:

  • Semmes-Weinstein 10 g monofilaments
  • Vibration thresholds
  • Ankle reflexes
  • Vascular checks
  • Pinprick test
  • Skin integrity reviews for deformity or callus.

A key diagnostic marker is infrared thermometry, where a temperature disparity exceeding 2°C between feet indicates active CNO.[9]

For investigations:[19]

  • Bilateral weight-bearing radiographs are the first-line tool, but may appear normal in early stages.
  • MRI is the most sensitive modality for detecting Stage 0 bone marrow oedema and distinguishing CNO from osteomyelitis.[3]
  • If MRI is contraindicated, bone scintigraphy or SPECT-CT are viable alternatives.[20]
  • While inflammatory markers like C-Reactive Protein and Erythrocyte sedimentation rate are typically only mildly raised in CNO, significantly elevated levels suggest concurrent infection.

[21]

Differential Diagnosis

There is a high rate of misdiagnosis in patients with CNO, which delays treatment and worsens outcomes. The most important conditions to differentiate are:[2][12]

Treatment

Medical Management

Conservative Management

It can take several months to treat CNO. The first-line treatment for suspected active CNO is a non-removable knee-high device, such as a total contact cast (TCC), which should be initiated immediately without waiting for imaging.[22] If a patient cannot tolerate a total contact cast, a removable knee-high device rendered irremovable is a suitable alternative. Evidence indicates that weight-bearing within these casts does not adversely affect healing, making it a viable option for selected patients.[23]

A Charcot restraint orthotic walker (CROW)is used to stabilise the deformities of the foot and ankle and minimise bone & joint destruction. It features a rocker-bottom sole and total-contact design that immobilises the joints and allows patients to ambulate. Foot casts and braces could be worn for 2-3months. Depending on the patient's compliance and the stage of the disease, both weight-bearing and non-weight-bearing regimens can be successful.[23] Immobilisation typically lasts three to six months, during which time bone repair is verified and inflammation is monitored continuously.[22] Serial monitoring of skin temperature differential (affected vs. contralateral foot) using infrared thermometry guides safe withdrawal of offloading; a temperature difference of less than 2°C on two successive visits 2–4 weeks apart supports transition to the next level of activity.[9]

Walking aids and wearing shoes that fit feet properly[24] There are other ways to manage symptoms and limit progression conservatively. These strategies, along with lifestyle modifications, may help prevent new problems and deterioration.

Surgical Management

When conservative treatment is ineffective, or there is a significant deformity that orthotic devices are unable to address, surgery may be required. The goals of surgery are to realign the foot architecture, stabilise fractured bones or dislocated joints, and provide a plantigrade, braceable foot that can support the proper footwear. [25] Exostectomy (removal of bony prominences), arthrodesis (fusion of affected joints), and Achilles tendon lengthening to lessen forefoot pressure are common operations. [25][18].

Surgical management of CNO has evolved significantly over the last decade through the use of minimally invasive techniques, super construct fixation, and computer-navigated correction.[26] Retrospective data indicate that procedures such as tendon balancing and subtalar arthrodesis can yield favourable long-term results for carefully selected patients, especially when performed after the acute inflammatory phase has subsided.[27] Although there is no one ideal anchoring technique, surgical reconstruction provides a feasible limb salvage alternative with low amputation risk for certain individuals. However, due to scanty controlled studies and inconsistent reporting of results, the overall quality of the evidence remains low.[28]

Surgical reconstruction is generally reserved for Stage 2 or 3 disease, once bone consolidation has occurred, although emergency surgery may be necessary for severe instability or infection.[29] Moreover, approximately 60% of cases after the initial treatment and over 90% of cases overall were successful, according to a systematic evaluation of plantar exostectomy; however, surgeries carried out below the lateral column were linked to a greater rate of various sequelae.[30]

Post-operative care incorporates a period of non-weight bearing followed by progressive protected weight bearing, with patients subsequently transitioned into accommodative bracing such as a CROW or ankle-foot orthosis, and thereafter into depth-inlay shoes with custom foot orthoses; management following removal of a CROW should incorporate lifelong protection of the extremity, including both patient education and professional foot care. Ongoing surveillance is essential to identify new ulcerations or the recurrence of deformity.[29]

Wound Care Management

Clinicians initiate wound care management when a plantar or perimalleolar ulcer fails to progress towards healing despite adequate offloading. Wound care principles align with diabetic foot infection management per IWGDF guidelines:[31][32]

  • Regular debridement of callus and necrotic tissue
  • Appropriate dressing selection based on wound characteristics (moisture balance, infection status)
  • Clinicians should hospitalise and treat with intravenous (IV) antibiotics when infection is life-threatening; deep tissue or bone culture should guide antibiotic selection
  • Negative pressure wound therapy may be considered for complex wounds following surgical debridement

Physiotherapy

As part of a multidisciplinary team, physiotherapists are vital to managing CNO through all stages of care. During the active phase, they monitor offloading adherence and disease activity using serial infrared thermometry.[3]

Physiotherapists also focus on maintaining independence and preventing deconditioning during immobilisation. They manage mobility aids, upper limb function, and prescribe seated aerobic exercises to support cardiovascular health and glycaemic control. [33]As the condition reaches remission, the focus shifts to graduated weight-bearing and gait rehabilitation.[34] This transition aims to correct compensatory patterns that increase ulceration risk. Strengthening exercises for the core and lower limbs help redistribute plantar loading forces. Furthermore, targeted balance and proprioceptive training are essential to reduce fall risks associated with neuropathy, utilising weight-shifting and low-impact options like hydrotherapy to improve functional outcomes.[35]

A study found TENS might be effective for pain treatment in diabetic neuropathy.[36] The systematic review concluded that Low-level laser therapy has a positive effect on neuropathic pain.[37]

Post surgical rehabilitation, as well as rehabilitation process after an amputation are also part of the care physiotherapy provides.

For further reading, the topics below expand on what physiotherapy can offer in CNO management.

Patient education

Physiotherapists and other MDT members should provide structured education to people with CNO and their carers. The following guidance should be delivered in the context of an individualised care plan and documented accordingly. It is recommended that education be tailored to the health literacy level and cultural context.

Clinicians should advise people with CNO and those at risk of CNO to:[38][39][40]

  • Inspect both feet daily, including the plantar surface and between the toes, using a mirror if necessary
  • Bathe feet in lukewarm water (test temperature with the elbow, not the foot, due to sensory impairment)
  • Dry carefully between the toes after washing
  • Apply a moisturising cream to the dorsal and plantar foot surfaces (avoiding between the toes)
  • Never walk barefoot, including indoors
  • Wear properly fitting, prescribed therapeutic footwear or custom-made orthotic devices
  • Report any unilateral swelling, redness, warmth, or skin breakdown immediately to their specialist foot team and not to wait for pain
  • Adhere strictly to the offloading regimen prescribed; removing the device prematurely significantly increases the risk of deformity progression
  • Maintain optimal glycaemic control in consultation with their diabetes care team
  • Attend all scheduled follow-up appointments and monitor foot temperature at home if instructed to do so.

Prognosis

CNO carries significant long-term morbidity, and prognosis is hinged on certain considerations. The active phase typically requires 3–12 months or longer of immobilisation; individual duration varies considerably and is guided by successive clinical and thermometric assessment.[2] A retrospective cohort study of patients with early-stage CNO (Eichenholtz Stage 0–1) managed with TCC found that early intervention with total offloading achieved remission in the majority of patients and avoided major amputation at 12 months.[41] The risk of major amputation increases substantially once plantar ulceration and osteomyelitis develop.[2]

Moreover, CNO can reactivate following remission, particularly in the first two years; ongoing surveillance and footwear management are essential.[42] Worthy of note is that up to 30% of people with CNO develop the condition in the contralateral limb; bilateral surveillance is therefore essential.[3][42] In addition, surgical reconstruction (hindfoot arthrodesis) carries high complication and reoperation rates in non-plantigrade deformity, emphasising the importance of preventing deformity through early conservative management.[43] Finally, CNO significantly affects mobility, independence, and mental health; MDT-led rehabilitation addressing physical, psychological, and social domains is essential for optimising long-term quality of life.[44]

Summary

Charcot neuro-osteoarthropathy is a limb-threatening complication of peripheral neuropathy, typically caused by diabetes, that leads to progressive bone destruction and joint deformity. Because a unilateral hot, swollen foot is frequently misidentified as cellulitis or deep vein thrombosis, clinicians must have a high index of suspicion to avoid diagnostic delays. The primary management strategy involves immediate offloading with a non-removable knee-high device as soon as CNO is suspected, rather than waiting for imaging. Throughout this process, infrared thermometry serves as a practical tool for monitoring disease activity and guiding the safe return to weight-bearing.

Effective care requires a multidisciplinary approach where physiotherapists provide essential support across all stages, from maintaining function during immobilisation to gait and balance rehabilitation guided by IWGDF 2023 standards. Since patients face permanent risks of reactivation, contralateral involvement, and ulceration, long-term follow-up is mandatory.[42] Ultimately, a person-centred model that addresses the physical, social, and psychological burdens of the disease is necessary to ensure optimal quality of life and limb preservation.

References

  1. ↑ 1.0 1.1 1.2 Greco T, Mascio A, Comisi C, Polichetti C, Caravelli S, Mosca M, et al. RANKL-RANK-OPG pathway in Charcot diabetic foot: pathophysiology and clinical-therapeutic implications. Int J Mol Sci. 2023; 24(3):3014. doi:10.3390/ijms24033014.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Bell DSH, Jerkins T. Diabetic Charcot neuroarthropathy: A threat to both limb and life. Diabetes Obes Metab. 2025; 27(1):35-39. doi: 10.1111/dom.15994.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Wukich DK, Schaper NC, Gooday C, Bal A, Bem R, Chhabra A, et al. Guidelines on the diagnosis and treatment of active Charcot neuro-osteoarthropathy in persons with diabetes mellitus (IWGDF 2023). Diabetes Metab Res Rev. 2024;40(3):e3646. doi: 10.1002/dmrr.3646.
  4. ↑ 4.0 4.1 Bansod H, Wanjari A, Dumbhare O. A Review on Relationship Between Charcot Neuroarthropathy and Diabetic Patients. Cureus. 2023;15(12):e50988. doi: 10.7759/cureus.50988.
  5. ↑ 5.0 5.1 Raspovic KM, Schaper NC, Gooday C, Bal A, Bem R, Chhabra A, et al. Diagnosis and treatment of active charcot neuro-osteoarthropathy in persons with diabetes mellitus: A systematic review. Diabetes Metab Res Rev. 2024; 40(3):e3653. doi: 10.1002/dmrr.3653.
  6. ↑ 6.0 6.1 Wukich DK, Frykberg RG, Kavarthapu V. Charcot neuroarthropathy in persons with diabetes: It's time for a paradigm shift in our thinking. Diabetes Metab Res Rev. 2024 Mar;40(3):e3754. doi: 10.1002/dmrr.3754.
  7. ↑ Stergioti A, Manganas K, Tzeravini E, Kosta O, Eleftheriadou I, Tentolouris A. Charcot Neuro-Osteoarthropathy in Diabetes: Implications for Diabetic Foot Ulcers, Amputations, and Survival. The International Journal of Lower Extremity Wounds. 2025 Dec;24(4):781-8.
  8. ↑ Jude EB, Siafarikas C, Rastogi A, Bem R, Tankova T, Kong MF, et al. Demographic and Clinical Characteristics of Patients With Charcot Neuro-Osteoarthropathy in People With Diabetes Mellitus in Six Countries: A Multicenter Observational Study From 1996 to 2022. J Diabetes Res. 2025; 2025:4275741. doi: 10.1155/jdr/4275741.
  9. ↑ 9.0 9.1 9.2 Dallimore SM, Puli N, Kim D, Kaminski MR. Infrared dermal thermometry is highly reliable in the assessment of patients with Charcot neuroarthropathy. J Foot Ankle Res. 2020; 13(1):56. doi: 10.1186/s13047-020-00421-z.
  10. ↑ Bagheri K, Anastasio AT, Krez A, Siewny L, Adams SB. Charcot Neuroarthropathy of the Foot and Ankle in the Acute Setting: An Illustrative Case Report and Targeted Review. West J Emerg Med. 2023;24(5):921-930. doi: 10.5811/westjem.59833.
  11. ↑ Tsatsaris G, Rajamand Ekberg N, Fall T, Catrina SB. Risk factors for Charcot foot development in individuals with diabetes mellitus. Diabetologia. 2024;67(12):2702-2710. doi: 10.1007/s00125-024-06271-9.
  12. ↑ 12.0 12.1 12.2 12.3 Martinazzi BJ, Manto KM, Dopke KM, Mansfield K, Walley K, Aynardi M. Charcot neuroarthropathy: current concepts. SurgiColl. 2024;2(2). doi:10.58616/001c.87829
  13. ↑ Fauzi AA, Chung TY, Latif LA. Risk factors of diabetic foot Charcot arthropathy: a case-control study at a Malaysian tertiary care centre. Singapore Med J. 2016;57(4):198-203. doi: 10.11622/smedj.2016074.
  14. ↑ Jiang S, Wang S. Analysis of Genetic Risk Factors Associated with Charcot Foot Based on the FinnGen Study R9 Data: A Wide-angle Mendelian Randomization Study. Int J Low Extrem Wounds. 2025; 24(4):814-827. doi: 10.1177/15347346241283260.
  15. ↑ Kaynak G, Birsel O, Fatih Güven M, Öğüt T. An overview of the Charcot foot pathophysiology. Diabetic foot & ankle. 2013;4(1):21117.
  16. ↑ JFootScientific. What Causes Charcot Foot? Available from: https://www.youtube.com/watch?v=MWhzy9Us3R0 [last accessed 30/04/2026]<
  17. ↑ Donald E. Pelto DPM. Charcot Foot - What YOU need to KNOW!. Available from: http://www.youtube.com/watch?v=d9_JIfbrbxk[last accessed 30/04/2026]
  18. ↑ 18.0 18.1 Bajuri MY, Ong SL, Das S, Mohamed IN. Charcot Neuroarthropathy: Current Surgical Management and Update. A Systematic Review. Front Surg. 2022; 9:820826. doi: 10.3389/fsurg.2022.820826.
  19. ↑ Mascio A, Comisi C, Cinelli V, Pitocco D, Greco T, Maccauro G, et al. Radiological Assessment of Charcot Neuro-Osteoarthropathy in Diabetic Foot: A Narrative Review. Diagnostics (Basel). 2025;15(6):767. doi: 10.3390/diagnostics15060767.
  20. ↑ Ahluwalia R, Bilal A, Petrova N, Boddhu K, Manu C, Vas P, et al. The Role of Bone Scintigraphy with SPECT/CT in the Characterization and Early Diagnosis of Stage 0 Charcot Neuroarthropathy. J Clin Med. 2020;9(12):4123. doi: 10.3390/jcm9124123.
  21. ↑ TYLER FOOT CLINIC. Charcot Foot. Available from: https://www.youtube.com/watch?v=FcoykAh16jk [last accessed 23/3/2021]
  22. ↑ 22.0 22.1 Berhane T, Jeyaraman K, Hamilton M, Falhammar H. Offloading Interventions for the Management of Charcot Neuroarthropathy in Diabetes. Foot Ankle Orthop. 2025;10(1):24730114251315670. doi: 10.1177/24730114251315670.
  23. ↑ 23.0 23.1 Prem R, Vignaraja V, Lewis T, Budair B. Weight bearing versus non-weight bearing total contact cast in the management of active Charcot foot: A systematic review. SAGE Open Med. 2024; 12:20503121241306957. doi: 10.1177/20503121241306957.
  24. ↑ Pinzur MS, Shields N, Trepman E, Dawson P, Evans A. Current practice patterns in the treatment of Charcot foot. Foot & ankle international. 2000 Nov;21(11):916-20.
  25. ↑ 25.0 25.1 Pinzur M. Surgical versus accommodative treatment for Charcot arthropathy of the midfoot. Foot Ankle Int. 2004; 25(8):545-9. doi: 10.1177/107110070402500806.
  26. ↑ Ong SL, Bajuri MY, Mazli N. Outcome of surgical fixation for midfoot Charcot neuroarthropathy: a systematic review. Malays Orthop J. 2023;17(1). doi:10.5704/MOJ.2303.004
  27. ↑ Khan O, Kavarthapu M, Edmonds M, Kavarthapu V. Surgical management of Charcot foot - The advancements over the past decade. J Clin Orthop Trauma. 2023 Dec 14;47:102317. doi: 10.1016/j.jcot.2023.102317.
  28. ↑ Ha J, Hester T, Foley R, Reichert ILH, Vas PRJ, Ahluwalia R, Kavarthapu V. Charcot foot reconstruction outcomes: A systematic review. J Clin Orthop Trauma. 2020 May-Jun;11(3):357-368. doi: 10.1016/j.jcot.2020.03.025.
  29. ↑ 29.0 29.1 Argyropoulos M, Wynell-Mayow W, Johnson O, Faroug R, Johal KS, Deol RS, et al. Charcot neuro-osteoarthropathy: a review of key concepts and an evidence-based surgical management algorithm. Front Clin Diabetes Healthc. 2024; 5:1344359. doi: 10.3389/fcdhc.2024.1344359.
  30. ↑ Fernández-Ospina NH, López-Moral M, Molines-Barroso RJ, García-Madrid M, García-Morales E, Lázaro-Martínez JL. Safety and Efficacy of Plantar Exostectomies for the Management of Diabetic Charcot Midfoot Deformity: A Systematic Review. Int J Low Extrem Wounds. 2025; 24(4):789-796. doi: 10.1177/15347346251359063.
  31. ↑ Senneville É, Albalawi Z, van Asten SA, Abbas ZG, Allison G, Aragón-Sánchez J, et al. IWGDF/IDSA Guidelines on the Diagnosis and Treatment of Diabetes-related Foot Infections (IWGDF/IDSA 2023). Clin Infect Dis. 2023:ciad527. doi: 10.1093/cid/ciad527. Epub ahead of print. Erratum in: Clin Infect Dis. 2024;79(1):286. doi: 10.1093/cid/ciae287.
  32. ↑ Chen P, Vilorio NC, Dhatariya K, Jeffcoate W, Lobmann R, McIntosh C, et al. Guidelines on interventions to enhance healing of foot ulcers in people with diabetes (IWGDF 2023 update). Diabetes Metab Res Rev. 2024; 40(3):e3644. doi: 10.1002/dmrr.3644.
  33. ↑ Martínez De Jesús FR, Carro GV, Cendejas Alatorre R, Torres GG, Aragón Carreño MP, Loaiza EZ, et al. Clinical Practice Recommendations for Diabetic Foot Attack: This is How We Do It: Guidelines from the Latin American Diabetic Foot Association (ALAPID). Global Wound Care Journal. 2025; 1(2 Suppl. 1): S1–S54.
  34. ↑ McCarthy M, Yates T, Webb D, Game F, Gray L, Davies MJ. Health impacts of seated arm ergometry training in patients with a diabetic foot ulcer: protocol for a randomised controlled trial. BMJ Open. 2020;10(6):e039062. doi: 10.1136/bmjopen-2020-039062.
  35. ↑ Alissa N, Shipper AG, Zilliox L, Westlake KP. A Systematic Review of the Effect of Physical Rehabilitation on Balance in People with Diabetic Peripheral Neuropathy Who are at Risk of Falling. Clin Interv Aging. 2024;19:1325-1339. doi: 10.2147/CIA.S459492.
  36. ↑ Dubinsky RM, Miyasaki J. Assessment: Efficacy of transcutaneous electric nerve stimulation in the treatment of pain in neurologic disorders (an evidence-based review) Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2010;74(2):173-6.
  37. ↑ Anju M, Ummer V S, Maiya AG, Hande M. Low level laser therapy for the patients with painful diabetic peripheral neuropathy - A systematic review. Diabetes Metab Syndr. 2019; 13(4):2667-2670. doi: 10.1016/j.dsx.2019.07.035.
  38. ↑ Reiber GE. Diabetic foot care. Financial implications and practice guidelines. Diabetes care. 1992;15:29-31.
  39. ↑ Bakker K, Apelqvist J, Schaper NC, International Working Group on the Diabetic Foot Editorial Board. Practical guidelines on the management and prevention of the diabetic foot 2011. Diabetes/metabolism research and reviews. 2012;28:225-31.
  40. ↑ Pinzur MS, Slovenkai MP, Trepman E, Shields NN. Guidelines for Diabetic Foot Care: Recommendations Endorsed by the Diabetes Committee of the American Orthopaedic Foot and Ankle Society. Foot & Ankle International. 2005;26(1):113-119.
  41. ↑ Bittante C, Cerasari V, Bellizzi E, Ahluwalia R, Di Venanzio M, Giurato L, et al. Early Treatment of Acute Stage 0/1 Diabetic Charcot Foot Can Avoid Major Amputations at One Year. J Clin Med. 2024; 13(6):1633. doi: 10.3390/jcm13061633.
  42. ↑ 42.0 42.1 42.2 Gratwohl V, Jentzsch T, Schöni M, Kaiser D, Berli MC, Böni T, et al. Long-term follow-up of conservative treatment of Charcot feet. Arch Orthop Trauma Surg. 2022;142(10):2553-2566. doi: 10.1007/s00402-021-03881-5.
  43. ↑ Regauer M, Grasegger V, Fürmetz J, Kussmaul AC, Böcker W, Ehrnthaller C. High rate of complications after corrective midfoot/subtalar arthrodesis and Achilles tendon lengthening in Charcot arthropathy type Sanders 2 and 3. Int Orthop. 2023;47(1):141-150. doi: 10.1007/s00264-022-05567-y.
  44. ↑ Gooday C, Hardeman W, Game F, Woodburn J, Poland F. A qualitative study to understand people's experiences of living with Charcot neuroarthropathy. Diabet Med. 2022;39(6):e14784. doi: 10.1111/dme.14784.
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